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Increased Mer and Axl receptor tyrosine kinase expression on glomeruli in lupus nephritis

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Abstract

Mer and Axl receptor tyrosine kinases (MerTK and AxlTK) play important roles in the clearance of apoptotic cells and the inhibition of inflammatory responses. Previous studies demonstrated that they might participate in glomerular injury in mice model. This study aimed to elucidate the expression of MerTK and AxlTK on glomeruli and analyze their clinical significance in lupus nephritis (LN) patients. Twenty-nine LN and 10 primary nephrotic syndrome (NS) patients were recruited. The expression of MerTK and AxlTK on glomeruli was measured by immunohistochemistry. Correlations between the levels of MerTK and AxlTK and clinical data were investigated. Statistical differences in each group were calculated by one-way analysis of variance, t test, or Mann-Whitney U test. Correlations were evaluated with Pearson’s or Spearman’s correlation tests. Both MerTK and AxlTK were expressed mainly on mesangial cells. LN patients demonstrated more expression of MerTK and AxlTK than primary NS patients (1.19 ± 1.01 × 10−2 vs 0.21 ± 0.29 × 10−2, 7.25 ± 2.69 × 10−2 vs 3.10 ± 1.22 × 10−2, p < 0.01). In LN patients, MerTK expression correlated with AxlTK (r = 0.529, p < 0.01). LN patients with class IV expressed more MerTK and AxlTK (1.50 ± 1.03 × 10−2 and 7.56 ± 2.93 × 10−2). The expression of MerTK and AxlTK varied according to the deposition of immunoglobulin and complements on glomeruli. Both MerTK and AxlTK expressions were increased on glomeruli and varied according to pathological classifications. Thus, we assumed that both two subsets might participate in the pathogenesis of LN.

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Acknowledgements

The work was supported by a grant from the National Natural Science Foundation of China (81172844 and 81471600).

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Correspondence to Yin Su or Bao Dong.

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Shanshan Li and Qianyu Guo contributed equally to this work.

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Li, S., Guo, Q., Zhu, H. et al. Increased Mer and Axl receptor tyrosine kinase expression on glomeruli in lupus nephritis. Clin Rheumatol 36, 1063–1070 (2017). https://doi.org/10.1007/s10067-017-3550-8

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